The role of cholesterol oxidation products in atherogenesis has long been a controversial topic. Peng and Taylor (1983), for example, argue that cholesterol oxidation products may be responsible for an initial arterial cell injury that eventually results in atherosclerosis. On the other hand, Higley et al. (1986) claim that oxidized cholesterol is substantially less atherogenic than purified cholesterol. Peng and Taylor, in Perkins and Visek, eds., "Dietary Fats and Health" (American Oil Chemists Society, Champaign, Ill., 1983), pp. 919-933; and Higley et al. (1986), Atherosclerosis, 62:91-104.
Hypercholesteroloemia is widely considered to be a major risk factor for the development of atherosclerosis. The lowering of blood cholesterol levels has therefore been an important goal in the search for ways to prevent or treat atherosclerosis. Medicinal agents reported as reducing development of athersclerotic lesions typically result in the lowering of blood cholesterol levels. Beneficial agents which do not affect blood cholesterol are rare. But Bell and Schaub (1986) have reported that chlorpromazine reduced the development of such lesions in rabbits fed an atherogenic diet without lowering of blood cholesterol. Chlorpromazine may function as an inhibitor of calmodulin (Gietzen, 1986), but it is classified pharmacologically as a tranquilizer and sedative (Merck Index, 1976, page 280), and therefore is not likely to be useful as a treatment for atherosclerosis. Bell and Schaub (1986), Arteriosclerosis, 6:42-48; and Gietzen (1986), in Baker, et al., eds. "Intracellular Celcium Regulation" (Manchester University Press, Manchester, U.K.), pp. 405-423.